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It is currently postulated that IDO1, IDO2, and TDO activity can cause near total depletion of cellular tryptophan, which in turn triggers an accumulation of uncharged tRNAs and consequently activates the GCN5 kinase pathway and causes T cell dysfunction [75]
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Its two biologically active forms serve distinct biochemical roles: methylcobalamin sustain the metabolism critical for nucleic acid synthesis and methylation reactions
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